Retinol (vitamin A) inhibits sister chromatid exchanges and cell cycle delay induced by cyclophosphamide and aflatoxin B1 in Chinese hamster V79 cells.
Retinol (vitamin A alcohol) at the doses tested neither induced an increase of frequency of sister chromatid exchanges (SCE) nor cell cycle delay in Chinese hamster V79 cells with or without the metabolic activation of S-9 mix. However, it inhibited SCE frequencies and cell cycle delay in V79 cells induced by the indirect mutagen cyclophosphamide or aflatoxin B1. The inhibition was found to be dose and time dependent. These results suggest that retinol itself may have no direct effect on the genetic materials but rather exert its effects possibly by inhibiting the metabolic activation of an indirect mutagen or carcinogen. Thus, the antitumor activities of retinoids may not be limited to the widely accepted role of preventing the promotion step but also the initiation step of carcinogenesis.
D016604:Aflatoxin B1; D000348:Aflatoxins / Q000633:toxicity*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D002453:Cell Cycle / Q000187:drug effects*; D002460:Cell Line; D006224:Cricetinae; D003412:Cricetulus; D003434:Crossing Over, Genetic / Q000187:drug effects*; D003520:Cyclophosphamide / Q000633:toxicity*; D012854:Sister Chromatid Exchange / Q000187:drug effects*; D014801:Vitamin A / Q000494:pharmacology*
D000348:Aflatoxins; D000970:Antineoplastic Agents; D014801:Vitamin A; D003520:Cyclophosphamide; D016604:Aflatoxin B1